A shift from reversible to irreversible X inactivation is triggered during ES cell differentiation.

By Anton Wutz, R. Jaenisch. Molecules and Cells, 2000

607 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4312d18f3698b699d92fe67e23fed37e96ff5369

How researchers see this paper

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In Genetics

1. E. Li
2. A. Bird
3. Wolf Reik
4. Edith Heard
5. R. Jaenisch
6. C. D. Allis
7. M. Blasco
8. Stefan Schoeftner

In Molecular Biology

1. Yi Zhang
2. A. Bird
3. E. Li
4. Howard Y. Chang
5. C. D. Allis
6. Wolf Reik
7. T. Jenuwein
8. M. Blasco

Citations in the corpus

• Chromosomal silencing and localization are mediated by different domains of Xist RNA (2002, background): “and an Xist cDNA, establishing Xist as a crucial regulator of X inactivatio”
• Histone and chromatin cross-talk. (2003, background): “Upregulation of Xist expression followed by global Xist coating of the chromosome that is going to be silenced are the earliest events in the X-inactivation process (a ‘cis’-limited effect) [94].”
• Polycomb group proteins Ring1A/B link ubiquitylation of histone H2A to heritable gene silencing and X inactivation. (2004, methodology): “Previous studies have shown that expression of Xist transgenes in undifferentiated ES cells is sufficient to induce gene silencing and many of the chromatin modifications associated with X inactivation (Wutz and Jaenisch, 2000; Kohlmaier et al., 2004).”
• Chromatin modification and epigenetic reprogramming in mammalian development (2002, background): “Inducible expression of an Xist cDNA transgene in male ES cells is sufficient to trigger the inactivation of an autosome, in which the Xist transgene is integrated, which leads to the hypoacetylation of histone H4 and to the late replication of this chromosom”
• DNA methylation patterns and epigenetic memory. (2002, background): “In placental mammals, repression of X-linked genes follows expression of Xist, which sets in train the inactivation process, culminating in widespread methylation of CpG islands.”
• A novel role for Xist RNA in the formation of a repressive nuclear compartment into which genes are recruited when silenced. (2006, background): “Xist RNA coating of the X chromosome induces inactivation rapidly, within one or two cell cycles (Penny et al. 1996; Marahrens et al. 1998; Wutz and Jaenisch 2000).”
• Establishment of histone h3 methylation on the inactive X chromosome requires transient recruitment of Eed-Enx1 polycomb group complexes. (2003, background): “Finally, Eed-Enx1 complexes are not re- differentiation stages (Wutz and Jaenisch, 2000).”
• Xist nucleates local protein gradients to propagate silencing across the X chromosome (2021, methodology): “Genotyping and confirmation of deletion of the B-repeat in both cell lines and targeting on the 129 allele in F1 2-1 ESCs were performed by Southern blotting (not shown).”
• Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals (2003, background): “By contrast, DNA methylation seems not to be involved in establishing X inactivation because Xist activation and late replication precedes de novo methylation of CpG islands by a few day”
• Time-resolved structured illumination microscopy reveals key principles of Xist RNA spreading (2020, background): “Xist transgenes expressed from ectopic autosomal locations recapitulate Xist RNA functions, including chromosome silencing in cis (3, 4).”